Thursday, August 19, 2010

New at PLoS ONE: From Grazing Resistance to Pathogenesis: The Coincidental Evolution of Virulence Factors

Sandrine Adiba et al., 2010. PLoS ONE 5(8): e11882. doi:10.1371/journal.pone.0011882


"If you happen to be stranded in a building, it's probably not the occasion to start setting fire to things. But this is perhaps what some bacteria do when they find themselves challenged inside a human; they cause then the diseases that are potentially fatal but not contagious. Loosing thus an opportunity to escape (transmission), they risk getting perished with their host. This seems like a ludicrous strategy but we're looking at it from the wrong perspective – our own. By analogy, we just suffer a collateral damage in an invisible war (caution: this is an oversimplification of the process!). Like all living things, bacteria have to protect themselves against predators such as protists (amoebae). Some microorganisms do so by turning their repertoire of certain genes on, and, by that, they transform them from passive victims into aggressive fighters. And by coincidence, these same adaptations make them more virulent (better survival advantage and colonization traits) in human bodies. We're just caught in the crossfire! " (in syndication with

Read the abstract of Adiba et al., below:

To many pathogenic bacteria, human hosts are an evolutionary dead end. This begs the question what evolutionary forces have shaped their virulence traits. Why are these bacteria so virulent? The coincidental evolution hypothesis suggests that such virulence factors result from adaptation to other ecological niches. In particular, virulence traits in bacteria might result from selective pressure exerted by protozoan predator. Thus, grazing resistance may be an evolutionarily exaptation for bacterial pathogenicity.

This hypothesis was tested by subjecting a well characterized collection of 31 Escherichia coli strains (human commensal or extra-intestinal pathogenic) to grazing by the social haploid amoeba Dictyostelium discoideum. We then assessed how resistance to grazing correlates with some bacterial traits, such as the presence of virulence genes. Whatever the relative population size (bacteria/amoeba) for a non-pathogenic bacteria strain, D. discoideum was able to phagocytise, digest and grow. In contrast, a pathogenic bacterium strain killed D. discoideum above a certain bacteria/amoeba population size. A plating assay was then carried out using the E. coli collection faced to the grazing of D. discoideum. E. coli strains carrying virulence genes such as iroN, irp2, fyuA involved in iron uptake, belonging to the B2 phylogenetic group and being virulent in a mouse model of septicaemia were resistant to the grazing from D. discoideum. Experimental proof of the key role of the irp gene in the grazing resistance was evidenced with a mutant strain lacking this gene. Such determinant of virulence may well be originally selected and (or) further maintained for their role in natural habitat: resistance to digestion by free-living protozoa, rather than for virulence per se.

This is an Open Access article and available therefore free of cost from PLoS ONE journal website.

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